Porcine reproductive and respiratory syndrome virus (PRRSV) is a member of the virus family Arteriviridae and belongs, together with the Coronaviridae, to the virus order Nidovirales. PRRSV is an enveloped virus with a single-stranded, positive-sense RNA genome of about 15 kilobases comprising nine open reading frames (ORFs), namely ORF1a, ORF1ab, ORF2a, ORF 2ab, and ORFs 3 through ORF7. ORFs 1a and 1ab encode large polyproteins that are processed into the viral nonstructural proteins (nsp) by auto- and transcleavages of viral proteases nsp1, nsp2, and nsp4 (Snijder and Meulenberg, 1998).
There are two distinct viral PRRSV genotypes causing similar clinical symptoms that diverge by about 40% on nucleotide sequence level, genotype I (EU) and genotype II (US). The North American (US) prototype strain is VR-2332, while the European (EU) prototype strain is Lelystad virus.
PRRSV is considered one of the economically most important infectious agents in pigs causing late-term reproductive failure in sows and respiratory disease in growing pigs. Often, PRRSV infection is complicated by secondary bacterial infections being attributed to the immunosuppressive nature of the virus. Also, PRRSV viremia lasts for weeks, and virus then still can be detected in lymphoid organs for several months, demonstrating difficulties or failure of the host's immune response to clear the virus (Allende et al., 2000).
The specific immune response to PRRSV infection is characterized by delayed induction of neutralizing antibodies (Lopez and Osorio, 2004) and short cell-mediated immune response (Xiao et al., 2004). It is commonly accepted that these effects can in part be attributed, along with presentation of decoy epitopes (Ostrowski et al., 2002; Ansari et al., 2006) and glycan shielding of viral envelope proteins (Ansari et al., 2006), to the viral inhibition of the host's innate immune system. It has been demonstrated that PRRSV infection does not or only weakly or delayedly induce production of type I interferon (IFN) (interferon α and interferon β; (Miller et al., 2004)) or type II IFN, (interferon γ; (Meier et al., 2003)) in susceptible cell lines (swine pulmonary alveolar macrophages, monkey kidney cells MARC-145) and/or pigs (Buddaert et al., 1998).
Thus, there is a need for novel vaccines and medications effecting a rapid induction of neutralizing antibodies and interferon responses for the prophylaxis and treatment of PRRSV infection.